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TB:
Extrapulmonary
tuberculosis
(EPTB):
Tuberculosis can involve any organ system in the body.
While pulmonary tuberculosis is the most common
presentation, extrapulmonary tuberculosis (EPTB) is
also an important clinical problem.
Extrapulmonary tuberculosis (EPTB):
Isolated occurrence of TB at body sites other than the
lung
Extrapulmonary tuberculosis (EPTB) diagnosis:
At least one specimen with confirmed M. tuberculosis or
histological or strong clinical evidence consistent with
active EPTB
Case definition of an EPTB case with several sites
affected depends on: the site representing the most
severe form of disease
Pathogenesis:
Manifestations of EPTB:
Distribution of TB cases:
Distribution of tuberculosis cases by
anatomical site in HIV-negative patients
In immunocompetent adults,
it has been observed that
EPTB constituted about 15 to
20 per cent of all cases of
TB.
In HIV-positive patients, EPTB
accounts for more than 50
per cent of all cases of TB.
Presentation:
constitutional symptoms such as fever,
anorexia, weight loss, malaise and fatigue.
In India patients with EPTB especially when
the disease is located at an obscure site,
may present with pyrexia of unknown
origin (PUO) and this may be the only
diagnostic clue in them.
symptoms and signs related to the organ
system involved and these are discussed
under the respective anatomic sites.
Lymph node
tuberculosis
Lymph node
tuberculosis
Historically, lymph node tuberculosis (LNTB)
Pathogenesis:
1. LNTB is considered to be the local manifestation of a
systemic disease whereas NTM lymphadenitis is thought to
be a truly localised disease.
. M. tuberculosis gains entry into the body via the respiratory
tract and undergoes haematogenous and lymphatic
dissemination.
. Hilar and mediastinal lymph nodes are initially involved.
. This may occur at the time of primary infection or may
occur later in life due to reinfection or reactivation of
previous infection. Sometimes, tonsil is an important portal
of entry.
2. In contrast NTM, gain entry into the lymph nodes directly
via oropharyngeal mucosa, salivary glands, tonsils, gingiva
or conjunctiva, and lymph node involvement represents a
localised disease.
Clinical presentation:
Tubercular lymphadenopathy
stages:
Stage 1-2 and 3
Stage 4 and 5
Diagnosis:
1. FNA: smear microscopy, TB
culture, histology,
2. GeneXpert
3. Radiological findings
.CT scan (for intrathoracic and
intraabdominal LN)
.CXR
Differential diagnosis:
D/D: In severely immunocompromised
patients, tuberculous lymphadenopathy
may be acute and resemble acute
pyogenic lymphadenitis.
In adults, the differential diagnosis of
tuberculous lymphadenopathy includes the
following: persistent generalized
lymphadenopathy (PGL), lymphoma, Kaposi
sarcoma, carcinomatous metastases,
sarcoid, and drug reactions (e.g. phenytoin).
Persistent generalized
lymphadenopathy (PGL):
PGL is a feature of HIV infection which develops in up
to 50% of HIVinfected individuals. It is of no
prognostic significance.There is no specific treatment.
The diagnostic criteria for PGL are as follows: lymph
nodes larger than
1 cm in diameter
in 2 or more extra-inguinal sites
for 3 or more months.
The nodes are non-tender, symmetrical, and often
involve the posterior cervical and epitrochlear nodes.
PGL may slowly regress during the course of HIV
infection and may disappear before the onset of AIDS.
Pleural TB:
Manifest as Pleural effusion or
empyema thoracis
Tuberculosis pleural effusion is
categorised as extrapulmonary
despite an intimate anatomic
relationship between pleura and
the lungs.
Pathogenesis:
Small subpleural focus ruptures into the pleural
space leads to Interaction between tubercle bacilli or
their specific components inducing a delayed
hypersensitivity reaction. (evidence suggests that
patients with TB pleural effusion have significantly
higher levels of IFN-Y in the pleural fluid as compared
to peripehral blood thus exhibiting localisation of
predominantly Th1-type immunity in the pleural
fluid)
Rupture of a cavity (with caseous material) into the
pleural space results in empyema thoracis.
Less often, rupture of caseous paratracheal lymph
nodes, paravertebral abscess or osteomyelitis of the
ribs can result in empyema thoracis.
Clinical Features:
Physical Examination:
Digital clubbing
Decreased air entry
Dull percussion of chest
Friction rub
Intercostal tenderness
Occasionally, tuberculosis empyema
may present as a chest wall mass or
draining sinus tract (tuberculosis
empyema necessitatis).
Diagnosis:
Adenosine deaminase:
Adenosine deaminase (ADA) is an enzyme of purine metabolism which
catalyses adenosine into inosine and is found in most human tissues
particularly in the lymphoid tissues.
ADA estimation has been found to be useful in the diagnosis of
tuberculosis pleural effusion and ascites.
High ADA levels have also been reported in effusions due to rheumatoid
arthritis, lymphoma, chronic lymphatic leukaemia, empyema,
parapneumonic effusions, and mesothelioma. The sensitivity and
specificity of ADA estimation in the diagnosis of EPTB is shown.
ADA exists as two isoenzymes, ADA1 and ADA2, each with unique
biochemical properties. The ADA1 isoenzyme is found in all cells with the
highest activity in lymphocytes and monocytes, whereas ADA2
isoenzyme appears to be found only in monocytes.
In tuberculosis pleural effusion, ADA2 isoenzyme is considered to be
primarily responsible for total ADA activity, while in parapneumonic
effusions, the ADA1 isoenzyme is the major isoenzyme of ADA. Thus,
measurement of individual isoenzyme of ADA can enhance the diagnostic
utility of ADA estimation in pleural effusions.
Abdominal tuberculosis
Hepatobiliary and pancreatic TB are rare and are often associated with
miliary tuberculosis, and occur more often in immunocompromised
patients.
The clinical manifestations are non-specific and depend on the site and
extent of disease. Anorexia, malaise, low grade fever, weight loss,
night sweats, malaena, pancreatic mass or abscess or obstructive
jaundice have all been described.
Pancreatic TB may present as acute or chronic pancreatitis or may
mimic malignancy.
Isolated splenic tuberculosis is very rare in immunocompetent
persons. Splenomegaly can occur in patients with disseminated/miliary
tuberculosis. Splenic tuberculosis presents as hypersplenism or splenic
abscess or as a solitary splenic lesion. Multiple tuberculosis abscesses
have been described in patients with HIV infection. Preoperative
Pathogenesis:
Haematogenous spread from primary
lung focus in childhood, with later
reactivation
Ingestion of bacilli in sputum
Direct spread from adjacent organs
Lymphatic spread
Diagnosis:
Imaging (CXR, plain Xray abdomen, barium enema,
sonar, CT abdomen
Colonoscopy
Laparoscopy
Ascites
Sonar findings in gastrointestinal and peritoneal
TB
Free or loculated intraabdominal fluid
Sliced bread sign
Lymphadenopathy (mixed, heterogeneous)
Bowel wall thickening
Pseudokidney sign
Neurological
tuberculosis
1.Tuberculosis meningitis
Tuberculous meningitis.
Axial contrast-enhanced T1-weighted magnetic
resonance (MR) image shows florid meningeal
enhancement that is most pronounced within the basal
cisterns.
Clinical features:
Highest incidence in the first three years of life
Gradual disease over 26 weeks (may be acute)
Prodromal phase: Vague illhealth, apathy, behavioral
changes, anorexia, irritability
Later headache, vomiting and fever
Focal neurological deficits and features of raised
intracranial tension may precede signs of meningeal
irritation.
Focal or generalised seizures, are encountered in 20 to 30
per cent of patients.
Cranial nerve palsies can occur in 20 to 30 per cent of
patients, the sixth nerve involvement being the most
common. Complete or partial loss of vision is a major
complication of TBM.
Diagnosis:
1. Imaging
2. Differential cell count, protein, glucose, ADA
3. TB microscopy/culture
4. (GeneXpert MTB/RIF)
5. CSF investigation:
. Lumbar puncture is hazardous if the patient has a focal
neurological deficit (cerebral space-occupying lesion) or if
fundoscopy shows papilloedema (raised intracranial
pressure). In these circumstances, a CT brain scan is helpful,
if available. Otherwise, it may be safer to start presumptive
treatment with anti-TB drugs rather than risk lumbar
puncture.
. Lumbar puncture is important for differentiating purulent
from TB meningitis. Always exclude cryptococcal meningitis
by CSF microscopy (India ink stain) and, if available, fungal
culture.
Pericardial tuberculosis
Pericardial involvement in tuberculosis may
result in
1. acute pericarditis,
2. chronic pericardial effusion,
3. cardiac tamponade or
4. pericardial constriction.
. In India, TB accounts for nearly two-thirds of the cases of
constrictive pericarditis.TB has been reported to be the cause
of acute pericarditis in four per cent of patients in the
developed world and 60 to 80 per cent of the patients in the
developing world.
Clinical features
TB pericarditis occurs most commonly in the third
to fifth decade of life.
The disease has an insidious onset and presents
with fever, malaise and weakness. The patients
may manifest pericardial rub, vague chest pain or
cardiomegaly on a chest radiograph.
Acute onset has been reported in 20 per cent of
patients and some patients can present with
cardiac tamponade.
Dyspnoea, cough, and weight loss are common
symptoms. Chest pain, orthopnoea and ankle
oedema occur in nearly 40 to 70 per cent of
patients.
Pericardial effusion:
Patients with TB pericarditis usually
present with chronic pericardial effusion.
Patients may also present acutely with
cardiac tamponade and may manifest
severe distress, retrosternal
compression, raised jugular venous
pressure (JVP) with blunt y descent,
distant heart sounds, pericardial rub and
pulsus paradoxus may be evident.
Chronic constrictive
pericarditis:
In patients with chronic constrictive pericarditis, the inflow of
blood is impeded due to thickened unyielding pericardium,
especially in the late diastole. Consequently, these patients have
systemic as well as pulmonary venous congestion
manifest exertional dyspnoea, orthopnoea, ankle oedema and
ascites. Tachycardia, raised JVP with a prominent y descent occur.
The JVP may rise further on inspiration (Kussmauls sign). Pulsus
paradoxus is seen in less than one-third of cases and signifies
presence of some fluid or a relatively elastic pericardium. A
systolic retraction of apex can be evident. A pericardial knock
may be present but murmurs are not common. The ascites is
disproportionate to the oedema (ascites praecox). Severe
elevation of venous pressure may result in congestive
splenomegaly and protein losing enteropathy resulting in
hypoalbuminaemia. After many years of hepatic venous
congestion cardiac cirrhosis may develop in some patients. The
disease worsens gradually and in chronic cases, significant
myocardial atrophy occurs due to extension of inflammation and
Diagnosis:
The diagnosis usually rests on
1. suggestive constitutional and
2. cardiovascular features and
3. investigation findings (ECG, CXR and
echocardiography).
. It is important to exclude uraemia
and Kaposi sarcoma.
Cardiovascular signs
tachycardia
low blood pressure
pulsus paradoxus
raised jugular venous pressure (JVP) with small amplitude "a" and "v"
waves
impalpable apex beat
quiet heart sounds
pericardial friction rub
signs of right-sided heart failure (e.g. hepatomegaly, ascites, oedema)
CXR
large globular heart
clear lung fields
pleural fluid
ECG
tachycardia
ST and T wave changes
low voltage QRS complexes
sometimes electrical
alternans (alternating positive
and negative R
waves, reflecting a heart that
moves with each beat within
the pericardial fluid)
Echocardiography
pericardial fluid
strands crossing between
visceral and parietal
pericardium
Pitfalls in diagnosis of
pericardial effusion
Clinicians have misdiagnosed
pericardial effusion as the following:
congestive cardiac failure;
hepatoma or amoebic liver abscess
(enlarged liver);
bilateral pleural effusions.
Pericardiocentesis
This is only safe under the following
conditions:
a) echocardiography has confirmed a
moderate to large pericardial
effusion;
b) the operator is experienced.
The signs may be subtle. Assess
carefully any patient with oedema
or ascites with the possibility of
pericardial effusion in mind.
Therapeutic pericardiocentesis is
necessary if there is cardiac
tamponade (acute life-threatening
cardiac impairment).
Differential diagnosis:
Genitourinary
tuberculosis
Genitourinary tuberculosis
(GUTB) complicates three to four per cent
Cutaneous tuberculosis
Tuberculosis in otorhinolaryngology
Otorhinolaryngological TB
constitutes less than five per
cent of all cases of EPTB.
Focus has shifted on to
otorhinolaryngological TB
with the advent of HIV
infection and AIDS.
Tuberculosis of larynx
In the present era, in countries where TB is highly endemic,
almost all patients with laryngeal tuberculosis have been found to
have radiological evidence of pulmonary TB and many of them
may be sputum smear-positive. On the contrary, in countries with
a low prevalence of tuberculosis, associated pulmonary
tuberculosis is rarely seen in patients with laryngeal TB.
Clinical features: Patients often present with hoarseness of voice.
Pain is also an important feature which may radiate to one or
both ears and may lead to odynophagia.
D/D:
1. Occasionally, patients may present with rapid onset of
hoarseness of voice similar to that encountered in acute viral
laryngitis.
2. Laryngeal tuberculosis may co-exist with carcinoma. Clinical
features of these conditions may overlap and the lesions may
look similar.
TB sialitis
TB sialitis is usually secondary to tuberculosis infection of
the oral cavity or primary pulmonary tuberculosis.
Primary infection of the salivary glands is also known,
but, is rare.
Parotid gland is most commonly involved.
Clinical presentation can be acute or chronic. Acute
presentation may resemble acute non-tuberculosis sialitis
and clinical differentiation may be difficult. Occasionally,
the diagnosis of tuberculosis may be a surprise following
surgery performed for a suspected salivary gland tumour.
Unsuspected tuberculosis parotid abscess may be
wrongly drained mistaking it to be a pyogenic abscess.
This may lead to the formation of a persistent sinus.
Ocular tuberculosis
Ocular involvement has described in 2 to 30 per cent of patients
with tuberculosis, and usually develops as a result of
haematogenous dissemination.
While tuberculosis can affect all the part of the eye, choroid is the
most commonly affected structure. Primary ocular tuberculosis
though has been described is extremely rare. Tuberculosis affects
the eyelids infrequently. Lupus vulgaris may spread to the face and
involve the eyelid.
Conjunctival tuberculosis and lupus vulgaris are the common
manifestations of primary tuberculosis while tuberculids and
phlyctenulosis occur in postprimary tuberculosis. Phlyctenulosis can
involve conjunctiva, cornea or lid margin.
CHOROIDAL TUBERCLES, when present, can provide valuable
diagnostic clues to life threatening forms of disseminated
tuberculosis such as miliary tuberculosis. These may be single or
multiple and vary in size from quarter of a disc diameter to several
disc diameters and are most frequently situated at the posterior
pole.
1.
2.
.
Disseminated/miliary
tuberculosis
Disseminated tuberculosis (DTB) refers to involvement of two
or more non-contiguous sites.
Results from either a recent primary infection or the erosion of
a tuberculous lesion into a blood vessel.
During primary infection,
small numbers of tubercle bacilli gain access to the circulation
through the lymphatics and disseminate to visceral sites
which have rich vascular supply and good oxygenation such
as the liver, spleen, bone marrow and the brain.
foci heal by calcification in a majority of the patients.
In the post-primary period,
acute miliary tuberculosis (MTB) can occur when these foci fail
to heal and progress. Later in life, reactivation of these latent
foci, caseation and erosion into blood vessels can result in
haematogenous embolisation and the development of MTB.
Clinical presentation:
Even in areas where TB is highly endemic, the diagnosis of MTB can be
difficult as the clinical symptoms have been subacute and non specific
and the chest symptoms can be obscure till late in the disease. Patients
present with constitutional features rather than respiratory symptoms.
Skin involvement in the form of erythematous macules and papules and
unusual manifestations such as ulcerative lesions have also been
described.
Neurological involvement in the form of meningitis or tuberculomas is
common.
Overt adrenal insufficiency at presentation, or during treatment has also
been described.
Patients present with constitutional features rather than respiratory
symptoms.They may have hepatosplenomegaly and choroidal tubercles
(fundoscopy).
Often the presentation is associated with fever of unknown origin and
wasting may be marked. Miliary TB is an underdiagnosed cause of endstage wasting in HIV-positive individuals.A high index of suspicion is
necessary.
Diagnosis:
CXR shows diffuse, uniformly distributed, small
miliary shadows. "Miliary" means "like small
millet seeds".The CXR can appear normal in
advanced cases because of severe
immunosuppression and therefore inability to
mount an inflammatory response.
Full blood count may show pancytopenia. Liver
function tests may be abnormal.
Bacteriological confirmation (smears or
mycobacterial culture) is sometimes possible
from sputum, cerebrospinal fluid, bone
marrow, liver or blood.
Differential Diagnosis:
The differential diagnosis includes the
following:
1. The syndrome of HIV wasting disease
(sometimes referred to as slim disease),
2. Bacteraemia (including typhoid fever),
3. disseminated carcinoma,
4. disseminated infection with "atypical"
mycobacteria, trypanosomiasis (in endemic
regions) and
5. connective tissue diseases.
Diagnosis
Part
Methodological issues
Definitive diagnosis of tuberculosis involves demonstration of
M. tuberculosis by microbiological, cytopathological or
histopathological methods.
Clinical presentation of EPTB is atypical. Especially when the
disease involves obscure occult sites, EPTB may not even be
considered in the initial list of differential diagnosis.
Further, invasive methods may have to be employed to
secure tissue/body fluids for analysis. Many times
representative tissue/body fluid may not be accessible.
Even when adequate tissue is procured, the pathological
findings may be suggestive of granulomatous infection
which encompasses a wide range of differential diagnoses
rather than definitive tuberculosis.
Therefore, the clinicians more often rely upon the clinical
impression, radiological and endoscopic appearances and
nonconventional diagnostic methods as evidence to diagnose
EPTB.
Principles of diagnosis
When EPTB is suspected as a possible diagnosis, every
attempt should be made to procure tissue/relevant body
fluid for diagnostic testing.
Most accessible tissue should be procured for
histopathological, cytopathological and micrbiological
diagnosis.
For example, when working up a patient with suspected
lymph node tuberculosis, the most easily accessible
representative peripheral lymph node should be excised
and subjected to diagnostic testing. Similarly,
cerebrospinal fluid (CSF) and ascitic fluid examination
provide most valuable diagnostic clue in patients with
neurological and peritoneal tuberculosis respectively.
Dose of PPD:
The standard 5-tuberculin unit (TU) dose
of PPD-S is defined as the delayed skin
test activity contained in a PPD-S dose of
0.1 mg/0.1 ml.
The standard test dose of a commercial
PPD preparation is defined as the dose of
the product that is biologically equivalent
to that contained in 5 TU of PPD-S (i.e., it
elicits reactions of equivalent size +/_
20%).
Precaution while
handling:
PPD, when diluted in a buffered diluent, is adsorbed in
varying amounts by glass and plastics. A small amount of the
detergent Tween 80 is added by the manufacturer to the
diluent for PPD to reduce adsorption.
To minimize reduction in potency by adsorption, tuberculin
should never be transferred from one container to another,
and skin tests should be given as soon after the syringe has
been filled as possible.
Following these procedures will also help avoid
contamination: test doses should always be removed from
the vial under strictly aseptic conditions, and the remaining
solution should be kept refrigerated (not frozen).
Tuberculin should be stored in the dark as much as possible
and exposure to strong light should be avoided.
Administration of Test:
The test is administered by injecting 0.1 ml of 5-TU PPD
intradermally (Mantoux method) into the volar or dorsal surface of
the forearm. Other areas may be used, but the forearm is preferred.
The use of a skin area free of lesions and away from veins is
recommended.
The injection is made using a one quarter- to one-half-inch, 27gauge needle and a tuberculin syringe.
The tuberculin should be injected just beneath the surface of the
skin, with the needle bevel upward or downward . A discrete, pale
elevation of the skin (a wheal) 6 to 10 mm in diameter should be
produced when the injection is done correctly.
If it is recognized that the first test was improperly administered,
another test dose can be given at once, selecting a site several
centimeters away from the original injection. A note in the record
should indicate the site chosen for the second test.
Reading of Test:
Tests should be read between 48 and 72 h after injection,
when the induration is maximum. Tests read after 72 h
tend to underestimate the true size of induration.
Reading should be performed in a good light, with the
forearm slightly flexed at the elbow.
The basis of reading is the presence or absence of
induration, which may be determined by inspection (from
a side view against the light as well as by direct light)
and by palpation.
For standardization, the diameter of induration should be
measured transversely to the long axis of the forearm
and recorded in millimeter. The absence of induration
should be recorded as 0 mm, not negative.
IGRA:
Interferon-y (IFN-y) is a cytokine
produced by activated T-lymphocytes.
It plays a fundamental role in the
immune response to tuberculosis.
High levels of IFN-y have been
reported in tuberculosis pleural
effusions, possibly related to in situ
stimulation of CD4+ T lymphocytes by
tuberculosis antigens.
1.
2.
3.
.
.
Cerebrospinal fluid:
Clear CSF with moderately raised cells and protein and
low glucose constitute the typical CSF picture of TBM.
However, these characteristics are shared by other forms
of chronic meningitis and partially treated pyogenic
meningitis.
In the presence of coexisting spinal meningitis and spinal
block the CSF may be xanthochromic.
If allowed to stand, a pellicle or cobweb may form,
indicating the presence of fibrinogen. The pellicle is
highly suggestive but not pathognomonic of TBM.
CSF protein has been reported to be normal in some
patients with AIDS and TBM.
CSF glucose levels are abnormal in the majority of cases,
being less than 40 per cent of the corresponding blood
sugar level. However, CSF glucose levels are never
undetectable as in patients with pyogenic meningitis.
Pericardial fluid:
Echocardiography, pericardiocentesis and examination
of pericardial fluid can help in confirming the
diagnosis of pericardial tuberculosis.
Urine:
The yield of urine examination by smear and culture
for detecting the tubercle bacillus is low probably
because of the intermittent shedding of the bacilli.
Nevertheless, in patients with suspected genitourinary
tuberculosis, urine examination is mandatory.
Imaging:
Plain radiograph:
The association of pulmonary tuberculosis assessed by the chest
radiograph in patients with various forms of EPTB is depicted.
In patients with pleural tuberculosis,
the chest radiograph usually reveals a unilateral pleural effusion.
Sometimes the pleural effusion or empyema can be encysted or
multiloculated.
Encysted effusion may be confused with a mass lesion of the
pleura, mediastinum, chest wall and lungs. Most often encystment
occurs in the costoparietal regions, usually along the posterior
parietal pleural surface on the right side.
A lateral decubitus film may be useful in dstinguishing
subpulmonic encystment from subpulmonic of free fluid as both
these conditions present with a raised hemidiaphragm with
convexity lateral than usual with or without a blunted
costophrenic angle. Very rarely, encysted mediastinal pleural
effusion can present as an unexplained bulge of the mediastinum.
tuberculosis.
If there is a high index of suspicion of the diagnosis of MTB and the chest
radiograph is atypical, it is suggested that high resolution computed
tomographic scan (HRCT scan) be done to support the diagnosis. HRCT
scan is superior to the conventional CT scan in defining the parenchymal detail.
Further, HRCT of the chest with contrast can also be useful in detecting lymph
nodal enlargement, calcification and pleural lesions.
reveals
cardiac catheterisation
Immunodiagnostic
methods
Applied
to
body
fluids:
Most often, enzyme linked immunosorbent
assay (ELISA) for detecting mycobacterial
Applied to blood:
Adenosine deaminase:
Interferon-Y:
Interferon-y (IFN-y) is a cytokine produced by activated
T-lymphocytes. It plays a fundamental role in the
immune response to tuberculosis. High levels of IFN-y
have been reported in tuberculosis pleural effusions,
possibly related to in situ stimulation of CD4+ T
lymphocytes by tuberculosis antigens. A few studies
have shown a better sensitivity and specificity of pleural
IFN-y levels as compared to ADA levels.
Other non-conventional tests:
Lysozyme, a bacteriolytic protein which is widely
distributed in body fluids and many cells is a marker of
general inflammatory response. Lysozyme estimation
has been found to help identifying tuberculosis pleural
effusion.
Molecular methods:
Of these, polymerase chain reaction (PCR) has
often been applied to the CSF and pleural fluid to
detect various sequences representing the DNA of
M. tuberculosis.
Though the diagnostic utility of PCR in blood,
other body fluids such as ascitic fluid, urine,
pericardial fluid, pus from cold abscesses, and
tissue biopsy specimens has been studied,
available evidence is far from convincing. These
test results must be interpreted in the appropriate
clinical situation with caution.
PCR alone must not be the sole evidence on
which antituberculosis treatment is initiated or
withheld.
Xpert Test:
The recently developed CE-marked Xpert MTB/RIF
(Xpert)test (Cepheid Inc.), based on nested real-time
PCR and molecular beacon technology, has been
shown to be
1. rapid, with a result for TB and RIF resistance in
under 2 h;
2. not prone to cross-contamination;
3. requires minimal biosafety facilities;
4. can be performed by technicians with little training;
5. and has a high sensitivity in smear-negative
pulmonary TB (the last factor being particularly
relevant for patients with HIV infection).
. These characteristics also make it a potentially
attractive tool for extrapulmonary specimens.
Treatment
Part: